Table 1.
Genetic engineered mouse models of PDAC arising in mature pancreatic duct cells.
| Gene promoter | Tumor suppressor loss/mutation | Pancreas histology | Reference |
|---|---|---|---|
| CK19CreERT; LSL-KrasG12D | No | Mostly normal pancreas with scattered PanIN lesions | Kevin C Ray, et al. PLoS One, 2011. |
| Hnf1bCreERT2; KrasG12D, TP53R172H/R172H | Yes | Development of invasive PDAC through High grade PanIN lesions | Bailey JM, et al., Oncogene, 2016. 35(32): p. 4282–8 |
| Sox9CreER; KrasLSL-12D; Trp53flox/flox | Yes | High Grade PanIN lesions and PDAC | Lee AYL, et al., Gut. 2018 |
| Ck19-CreER; Kras LSL-G12D/wt; Fbw7f/f | Yes | Development of invasive PDAC through non mucinous tubular lesions. | Ferreira RMM, et al., Cell Reports. 2017 |
| Sox9CreERT2; KrasG12D; Ptenflox/flox; R26RYFP | Yes | Pancreatobilliary type IPMN and invasive PDAC | Kopp JL, et al., Gastroenterology. 2018 |
| CK19CreERT2; LSL-KrasG12D; R26REYFP | |||
| Sox9CreERT2; LSL-KrasG12D; R26REYFP | |||
| with pancreatic duct ligation (chronic pancreatitis) | No | PDAC development through flat epithelial precursors. Few PanIN lesions observed. | Shi C, et al. CMGH, 2019. |